We investigated whether concurrent infection by hepatitis B virus (HBV) and hepatitis C virus (HCV) in China, a hyperepidemic area for these infections, was associated with a higher risk of causing hepatocellular carcinoma (HCC) than each infection alone in a metaanalysis in China, 32 case -control studies involving 3201 cases and 4005 controls, identified from a computer-based literature search from 1966 to 2004. The pooled odds ratio and 95% confidence interval (CI) for HBsAg positivity was 14.1 (95% CI: 10.6 -18.8); for anti-HCV/HCV RNA positivity was 4.6 (95% CI: 3.6 -5.9); for HBsAg positivity and anti-HCV/HCV RNA negativity were 15.6 (95% CI: 11.5 -21.3); for HBsAg negativity and anti-HCV/HCV RNA positivity were 8.1 (95% CI: 5.0 -13.0); and positivity for both HBsAg and anti-HCV/HCV RNA was 35.7 (95% CI: 26.2 -48.5). We conclude that HBV and HCV infections are important independent risk factors for HCC in China, and that dual infection by HBV and HCV is associated with a higher risk of causing HCC than each infection alone, suggesting a synergism between HBV and HCV. ). More than 500 000 new cases are currently diagnosed yearly, with an ageadjusted worldwide incidence of 5.5 -14.9 per 100 000 population (Llovet et al, 2003). About 110 000 persons die each year from HCC in China, which accounts for 45% of the deaths from HCC worldwide. China is also a hyperepidemic area for hepatitis B virus (HBV) infection (with an estimated carrier rate exceeding 10% in the general population) and hepatitis C virus (HCV) infection (with a prevalence of anti-HCV 3.1% of in the general population) (Xuezhong et al, 1999). HBV and HCV infections have each been shown to markedly increase the risk of developing HCC. In China, HBV has, for several decades, been the major cause of liver disease (Tang, 2001). Soon after the identification of HCV and the development of testing HCV infection, it has become increasingly evident that chronic HCV infection also plays an important role in chronic hepatic disease including HCC (Yano et al, 1993;Tsai et al, 1994). There have been several meta-analyses of the relation of HBV and HCV infections to HCC in China, but the relation of dual infection to HCC has not received similar attention. In fact, this is not rare in HCC patients and a higher morbidity in HCC patients with dual infection has been reported than in those with one infection (Benvegnu et al, 1994). The main difficulty in evaluating the relationship of dual infection to HCC is the rarity of concurrent infection in subjects without clinically evident liver disease. Only large case -control studies that include people unaffected by chronic liver diseases as controls can allow the interaction to be properly assessed. The aim of this meta-analysis is to assess the interaction between HBV and HCV infections among 32 casecontrol studies of HCC. MATERIALS AND METHODS Data sourcesWe searched the published Chinese literature from 1979 to February 2004 and Medline database from 1966 to February 2004 to identify case -control studies of the...

The mechanisms whereby hepatic fibrosis develops in chronic liver diseases remain incompletely defined. Here, we sought to examine whether microRNA (miRNA) became dysregulated in dimethylnitrosamine‐induced hepatic fibrosis in rats. Our microarray analysis revealed that the miR‐34 family was upregulated along with other miRNAs in liver fibrotic tissues. Six miRNAs, such as rno‐miR‐878, were downregulated. The findings were confirmed by RT‐PCR assays. Gene ontology analysis further showed that many of these dysregulated miRNAs were involved in lipid/fatty acid metabolism. The acyl‐CoA synthetase long‐chain family member 1 (ACSL1) gene contained specific binding sites for miR‐34a/miR‐34c. Additional enhanced green fluorescence protein reporter activity assays indicated that the miR‐34 family targeted ACSL1. Our RT‐PCR and immunoblotting assays further demonstrated that both the mRNA and protein levels of ACSL1 were markedly reduced in fibrotic liver tissues. Our findings suggest that miRNA becomes dysregulated during hepatic fibrosis, and that the miR‐34 family may be involved in the process by targeting ACSL1.

β-catenin, a core component of Wnt/β-catenin signaling, has been shown to be an important regulator of cellular proliferation and differentiation. Abnormal activation of Wnt/β-catenin signaling promotes tissue fibrogenesis. In the present study, the role of β-catenin during liver fibrogenesis was analyzed and the functional effects of β-catenin gene silencing in hepatic stellate cells (HSCs) using small interfering (si)RNA were investigated. The expression of β-catenin in human hepatic fibrosis tissues of different grades and normal human hepatic tissues was examined using immunohistochemistry. To inhibit the Wnt/β-catenin signaling pathway, siRNA for β-catenin was developed and transiently transfected into HSC-T6 cells using Lipofectamine 2000. β-catenin expression was evaluated by quantitative polymerase chain reaction (qPCR) and western blot analysis. The expression of collagen types I and III was evaluated by qPCR and immunofluorescent staining. Cellular proliferation and the cell cycle were analyzed using a methyl thiazolyl tetrazolium assay. Apoptosis was assessed by Annexin V staining. A higher expression level of β-catenin was identified in the patients with high-grade hepatic fibrosis in comparison with that of the normal controls. Additionally, β-catenin siRNA molecules were successfully transfected into HSCs and induced inhibition of β-catenin expression in a time-dependent manner. β-catenin siRNA treatment also inhibited synthesis of collagen types I and I in transfected HSCs. Furthermore, compared with those of the control group, siRNA-mediated knockdown of β-catenin in HSC-T6 cells inhibited cell proliferation and resulted in cell apoptosis. This study suggests a significant functional role for β-catenin in the development of liver fibrosis and demonstrates that downregulation of the Wnt/β-catenin signaling pathway inhibits HSC activation. Thus, this study provides a novel strategy for the treatment of hepatic fibrosis.

Needleless TEA improves major postoperative symptoms by enhancing vagal and suppressing sympathetic activities.